Hiroko Shinkai

Smooth Muscle Cells in the Development of Plasmatic Arterionecrosis, Arteriosclerosis, and Arterial Contraction

Plasmatic arterionecrosis, the causative lesion of hypertensive cerebral hemorrhage, follows upon medial muscle cell necrosis. The development of medial muscle cell necrosis, the earliest cerebral arterial change seen in hypertensive rats, was inhibited when these animals were fed a cholesterol and lard-supplemented diet. Insudation of fibrin was noted in the arterial intima of hypertensive rats with bilaterally constricted renal arteries. Removal of the constriction induced a fall in the elevated blood pressure and an increase of intimal muscle cells. These were responsible for the dissolution of the deposited fibrin, leading to arteriosclerosis. These myointimal cells may originate from the endothelium. Arterial contraction caused by methoxamine hydrochloride often induced the intrusion of one medial muscle cell into another and increased endothelial permeability. 12-24 h after contraction, the arterial segments showed medial muscle cell necrosis, endothelial desquamation with platelet adhesion, and blood plasma infiltration.

A Case of Malignant Duct‐Islet Cell Tumor of the Pancreas Immunohistochemical and Cytofluorometric Study

A rare duct‐islet cell tumor of the pancreas was studied using immunohistochemical, cytofluorometric and histo‐chemical methods. Histology and immunohistochemistry revealed that the tumor contained two distinct cell types; islet cell‐like neuroendocrine cells and exocrine duct cell components, suggesting an endodermal origin for both types. The cells showed marked pleomorphism and vascular and perineural invasion at the tumor periphery. Cytofluorometric study of the tumor cell DNA revealed an increased mean nuclear DNA content, without any aneuploidy. Histochemically, the tumor cells contained an increased number of argyrophilic nucleolar organizer regions (AgNORs) in their nuclei. The malignant potential of this duct‐islet cell tumor was suggested. Acta Pathol Jpn 41: 636‐641, 1991.

An electron microscopic study of plasmatic arterionecrosis in the human cerebral arteries

An electron microscopic study of the intracerebral arteries from 9 hypertensive cases was performed in order to elucidate the morphogenesis of the plasmatic arterionecrosis which was considered to be the direct cause of hypertensive intracerebral hemorrhage. In the preceding stage of the arterial lesions, marked necrosis of medial smooth muscle cells and increase of basement membrane-like substance in the intima and media were observed. The lumina of these arteries were slightly dilated. The dilatation and hemodynamic factors were supposed to cause endothelial injury resulting in blood plasma insudation into the intima through the opened spaces between endothelial cells. The insudated blood plasma dispersed and dissolved the basement membrane-like substance, collagen and elastic fibers in the arterial wall, leading to the development of the plasmatic arterionecrosis.

Retroperitoneal epithelioid angiomyolipoma leading to fatal outcome.

Epithelioid angiomyolipoma (AML) is a newly established variant of AML, characterized by monomorphous epithelioid cells that show HMB‐45 immunopositivity, and it often displays aggressive behavior. To date, they have mostly appeared in the kidneys; however, the present autopsy case of a 43‐year‐old female without the stigmata of tuberous sclerosis complex had a huge retroperitoneal mass, accompanied by involvement of the regional lymph nodes. Histopathologically, the tumor was composed of round, polygonal or short spindle‐shaped monomorphous cells with abundant eosinophilic cytoplasm and large nuclei with frequent multinucleation. Mitotic figures were scattered. Mature fat cells and thick‐walled abnormal blood vessels were totally absent. Immunohistochemically, the tumor cells were reactive with HMB‐45 and α‐smooth muscle actin antibodies. In spite of curative surgery and repeated radio‐ and chemotherapy, the tumor continued to grow and brought about the patients death 4 years after the initial symptoms. At autopsy, the peritoneal cavity was filled with the tumor mass exceeding 5.5 kg. Histopathological features were essentially the same as those of biopsy samples, but the cellular pleomorphism and emperipolesis were more easily identified. This report calls attention to this unusual manifestation of AML in the retroperitoneum and the importance of distinguishing it from sarcomas and/or paragangliomas.

Plasmatic arterionecrosis and its thrombotic occlusion

Abstract The vascular lesions directly responsible for hypertensive intracerebral hemorrhage were studied in autopsy cases, associated with some animal experiments. The immediate cause of the hemorrhage was the rupture of the intracerebral microaneurysms resulted from plasmatic arterionecrosis. At the beginning of the morphogenesis of the arterionecrosis, medial smooth muscle cells of the intracerebral arteries underwent necrosis and disappeared. Subsequently the lumen became somewhat dilated, followed by slight intimal thickening with fibrous tissue. In such intima occurred blood plasma insudation, which induced not only histolysis of the intimal tissue, but also intimal deposition of fibrinoid substance consisting mainly of fibrin. In the striate and thalamic arteries in the basal ganglia, the arterionecrosis and consequent microaneurysms occurred preferably at the bifurcations or in the somewhat distal segments from them. In the medullary arteries in the cortices, however, most of the microaneurysms were found in the just proximal segments from the rectangular bends at the cortico-medullary junction. But they were rarely seen in the straight medullary arteries without bending. These findings suggested the possible role of hemodynamics in the pathogenesis of the arterial lesions. The arterionecrosis was accompanied or not accompanied with the deposition of fibrinoid substance in the intima. In the latter occurred also histolysis due to blood plasma insudation and consequent microaneurysms. The intimal fibrinoid deposition, that is, fibrin deposition, could be considered, like mural thrombi, to have a biological significance of reinforcing the arterial wall that had been affected with marked histolysis. It seemed that microaneurysms most liable to rupture were those revealing the arterionecrosis with neither thrombosis nor dense deposition of abundant fibrin in the intima. The microaneurysms were sometimes occluded by thrombi and saved from rupture. The occluded lesions, however, were one of the causes of cerebral infarction. Twenty-six % of infarcts in the basal ganglia were caused by the occluded microaneurysms. The microaneurysms in the cortices were more liable to be occluded by thrombi than those in the basal ganglia, presumably because of the lower blood pressure in the former according to the law of Hagen-Poiseuille.